Contribution of the spinal cord BDNF to the development of neuropathic pain by activation of the NR2B-containing NMDA receptors in rats with spinal nerve ligation

Geng, Shan-Jing; Liao, Fei-Fei; Dang, Wenhao; Ding, Xu; Liu, Xiaodan; Cai, Jie; Han, Ji-Sheng; Wan, You; Xing, Guo-Gang

doi:10.1016/j.expneurol.2010.01.003

Cited by 142 publications

(114 citation statements)

References 96 publications

(129 reference statements)

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“…), the left L5 spinal nerve distal to the dorsal root ganglion (DRG) was tightly ligated with 4-0 silk sutures as described by Kim and Chung [13][14][15] . Animals were allowed to recover for 7 d before electrophysiological recordings.…”

Section: Snl Proceduresmentioning

confidence: 99%

Electrophysiological properties of spinal wide dynamic range neurons in neuropathic pain rats following spinal nerve ligation

Liu

Cai

et al. 2011

Neurosci. Bull.

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Objective The present study aimed to investigate the electrophysiological properties of wide dynamic range (WDR) neurons in spinal dorsal horn of rats with neuropathic pain induced by lumber 5 (L5) spinal nerve ligation (SNL) in a large size of samples. Methods Adult Sprague-Dawley rats were divided into normal and SNL groups. Electrophysiological technique was used to record the characteristics of WDR neurons in the spinal dorsal horn. Results Compared with the WDR neurons in normal rats, the WDR neurons in SNL rats showed an increase in excitability, manifested by an enlargement of the receptive field size, an increase in the proportion of neurons that exhibited spontaneous activities, decreases in the Cresponse threshold and latency, and an increase in the C-response duration. In addition, the numbers of A  -and C-fiberevoked discharges were smaller in SNL rats than in normal rats. Conclusion The excitability of spinal WDR neurons increased in rats with neuropathic pain induced by L5 SNL. The increase in excitability of WDR neurons may contribute to the development of neuropathic pain.

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Section: Snl Proceduresmentioning

confidence: 99%

Electrophysiological properties of spinal wide dynamic range neurons in neuropathic pain rats following spinal nerve ligation

Liu

Cai

et al. 2011

Neurosci. Bull.

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“…In models of pain after peripheral injury, there is evidence that p-p38 is active in association with microglial activation (Kim et al, 2002;Obata et al, 2004;Tsuda et al, 2004;Hains and Waxman, 2006;Trang et al, 2009). In addition, BDNF has been shown to be a key factor mediating the microglianeuron signaling and central sensitization (Coull et al, 2005;Geng et al, 2010). The signaling mechanisms between activated microglia and neurons that underlie enhanced postsynaptic excitability and changes in sensory processing after CIBP have not yet been established.…”

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confidence: 99%

Minocycline‐induced reduction of brain‐derived neurotrophic factor expression in relation to cancer‐induced bone pain in rats

Wang

Yang

et al. 2011

J of Neuroscience Research

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Previous studies have suggested that the release of brain-derived neurotrophic factor (BDNF) from microglia in spinal cord is necessary for maintaining pain hypersensitivity after nerve injury. However, little is known about its role in cancer-induced bone pain (CIBP), which is in some ways unique. This study demonstrates a critical role of minocycline (a potent inhibitor of microglial activation)-modulated BDNF in the induction and maintenance of behavioral hypersensitivity in a rat model of CIBP. We assessed mechanical threshold and spontaneous pain of CIBP rats. Moreover, minocycline was administered intrathecally from day 4 to day 6 (early stage) or from day 10 to day 12 (later stage), after carcinoma cell inoculation. Real-time PCR, Western blots, and double immunofluorescence were used to detect the expression of OX-42 (marker of activated microglia), phosphorylated p38-MAPK (p-p38), and BDNF. We found that intrathecal minocycline could prevent CIBP at an early stage of tumor growth (from day 4 to day 6). However, at the late stage (from day 10 to day 12), intrathecal minocycline had no effect. Moreover, the expression of OX-42 and BDNF under CIBP, peaking on day 6, were all reduced after minocycline injection from day 4 to day 6. The ability of minocycline-induced reduction of BDNF in the induction of behavioral hypersensitivity could provide an opportunity for alleviating CIBP.

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“…It contributes to both development and maintenance of neuropathic pain by activation of the dorsal horn NMDA-2B receptors. [72] It has been found that BDNF levels were significantly increased in the spinal dorsal horn in the spinal nerve ligation (SNL) rat model of NP. The maximal increase in BDNF expression was found in an early stage (24-48 hours) after SNL.…”

Section: Neurotrophins and Nerve Growth Factorsmentioning

confidence: 99%

Recent and Emerging Trends in Pharmacotherapy of Neuropathic Pain

Singh

Sehgal

Singh

2018

IJMDS

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Contribution of the spinal cord BDNF to the development of neuropathic pain by activation of the NR2B-containing NMDA receptors in rats with spinal nerve ligation

Cited by 142 publications

References 96 publications

Electrophysiological properties of spinal wide dynamic range neurons in neuropathic pain rats following spinal nerve ligation

Electrophysiological properties of spinal wide dynamic range neurons in neuropathic pain rats following spinal nerve ligation

Minocycline‐induced reduction of brain‐derived neurotrophic factor expression in relation to cancer‐induced bone pain in rats

Recent and Emerging Trends in Pharmacotherapy of Neuropathic Pain

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